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Atherogenic diet diminished endothelial glycocalyx contributes to impaired vasomotor properties in rat.

Hongyan Kang,Anqiang Sun,Qiuhong Wu,Jiali Yang,Weichen Zhang,Yuxin Qu,Menghan Gao,Xiaoyan Deng

Published 2020 in American Journal of Physiology. Heart and Circulatory Physiology

ABSTRACT

Hypercholesterolemia and atherosclerosis caused vasomotor properties dysfunction may be involved in many clinic manifestations of atherosclerosis, including angina, acute myocardial infarction, and sudden cardiac death. However, its underlying mechanism is not clear. The endothelial glycocalyx is a protective surface layer on the endothelial cells, serving as a molecular sieve, cell adhesion modulator, and mechanosensor for blood flow. In the present study, we demonstrated by confocal microscopy that the dimension of the endothelial glycocalyx reduced significantly in both the common carotid artery (2.89±0.41 µm and 3.25±0.44 μm, respectively) and the internal sinus region (2.35±0.07 µm and 3.46±0.86 μm, respectively) of the 12 week high cholesterol fed SD male rats (HC) as compared to the normal diet (NC). Furthermore, we showed by real time PCR that this dimension modification of endothelial glycocalyx may be attributed to a significant down-regulation of heparan sulfate proteoglycans (HSPG) related genes, including syndecan-3, glypican-1, and EXT1, not resulting from an enhanced shedding of sulfated glycosaminoglycans (sGAG) from the vessel wall to the plasma. Meanwhile, the mean contraction and relaxation forces of the common carotid artery with responses to norepinephrine (Ne) and acetylcholine (ACh) decreased approximately to 0.34 and 0.13 fold, respectively, accompanied by a lower level of nitric oxide (NO) release. These findings suggest that the atherogenic high cholesterol diet diminished endothelial glycocalyx and disturbed the local NO release, thus contributing to the impaired vasomotor properties of the vessel.

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